INTRODUCTION: In the years that followed the 1994 Back to Sleep Campaign (BSC), a public health initiative designed to prevent Sudden Infant Death Syndrome (SIDS), the prevalence of SIDS decreased by nearly 50%. However, recent research questions the decline in SIDS with an appreciation of contemporaneous factors which may have contributed to it. There is a growing recognition that other, often indiscernible causes of Sudden Unexpected Infant Deaths (SUID) have increased prevalence rates. Several researchers have addressed the possibility of the effects of a diagnostic drift. OBJECTIVE: To evaluate the impact of certain contemporaneous factors on the decline in the prevalence of Sudden Infant Death Syndrome. METHODS: We examined a historically significant time period surrounding the implementation of the BSC, 1984-2009. It is a time-period that incorporates mortality statistics prior to the BSC, as well as immediately following. We utilized 1984-2009 mortality data obtained from the Center for Disease Control and Prevention and evaluated the following prevalence rates: SIDS, unknown and unspecified causes, Accidental Strangulation and Suffocation in Bed (ASSB), and Neglect. We then amalgamated unknown and unspecified causes, ASSB and Neglect into a single representation of non-SIDS SUID. We then proceeded to perform an analysis on these prevalence rates to determine linear trends. RESULTS: All-cause mortality rate decreased linearly by about .929 per 100,000 per year (p<.0001, β=-.929). SIDS mortality rates also experienced a significant decline of about .951 per 100,000 deaths per year (p<.0001, β=-.951). In contrast, the SUID cohort prevalence increased significantly with a rate of .930 per 100,000 per year (p<.0001, β=.930). DISCUSSION: Over our study period, SIDS declined significantly, but by 2001 it experienced a stagnant decline that was different than that from 1984-2000. From 2001 to 2009, our SUID cohort increased dramatically. It is our conclusion that the potential exists for a possible diagnostic drift from SIDS to these other SUID.

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A brainstem-related abnormality in respiratory control appears to be one of the most compelling mechanisms for sudden infant death syndrome (SIDS). The elements calcium, copper, iron, potassium, magnesium, sodium, phosphorus, sulfur, and zinc were analyzed by inductively coupled plasma atomic emission spectroscopy in the brainstem of 30 infants who died from SIDS and 10 infants who died from other causes (control). No differences were found between SIDS and control for any element except for more calcium in the SIDS group. A multivariate analysis of the data failed to group the majority of SIDS and control subjects in different clusters. Further research is required to determine the biological significance of the higher calcium found in the SIDS group.,

Sudden Infant Death (SIDS) has been associated with medium-chain acyl-CoA dehydrogenase (MCAD) deficiency, an inborn error of fatty acid oxidation. Blood and tissue samples from a large cohort of SIDS victims were analyzed for the presence of dodecanoic acid (C₁₂) by gas chromatography. A subgroup of these cases had a significantly higher blood concentration than age-matched controls, suggesting MCAD deficiency. An animal study using Sprague-Dawley rats was done to mimic the effects of MCAD deficiency. Significantly increased blood concentrations of dodecanoic acid were observed. Decreased values in heart and liver were puzzling findings. The data indicate that dodecanoic acid is a blood marker for MCAD deficiency.

Thesis (MScMedSc)--University of Stellenbosch, 2011. / ENGLISH ABSTRACT: Sudden Unexpected Death in Infancy (SUDI) refers to any such sudden demise in a child. If the child dies while asleep within the first year of life, and if no conclusive cause of death can be ascertained by means of complete autopsy and investigation into the circumstances surrounding death, including visit of the death scene, such a case is classified as one of Sudden Infant Death Syndrome (SIDS). By South African law, a full medico-legal autopsy is mandated in cases where the cause of death is not evident – including cases of possible SIDS. There can be little doubt that viral infection can be a cause of death in cases of supposed SUDI. At the Tygerberg medico-legal (forensic) laboratory, the evaluation of lung tissue for the presence of fatal viral lung infections forms part of the institutional protocol for the examination of SUDI cases. Lung samples of these SUDI cases are routinely tested for the presence of Cytomegalovirus (CMV), adenovirus and respiratory syncytial virus (RSV) by means of shell vial cultures. In a retrospective pilot study of 366 SUDI case files from Tygerberg Hospital, Western Cape, from 2004 – 2006, it was evident that in only 13.9% of possible SIDS cases, positive results for one or more of the aforementioned viruses were obtained. We hypothesise that the current method of virus detection, together with other factors such as the interval between death and post mortem examination, transport time of the specimens to the laboratory etc. might not be optimal to give a realistic picture of death in infancy caused by viral pulmonary infection. As other test modalities exist for the diagnosis of pulmonary viral infections, these methods were compared in terms of positive yield and association with viral pneumonitis, keeping the cost and time needed for each assay in mind. A total of 82 samples were collected over an 8 month period and routine shell vial cultures were done, followed by real-time Polymerase Chain Reaction (PCR) and immunohistochemical (IHC) staining of the lung sections with consensus pathology opinion. As expected, the real-time PCR method was much more better suited for identifying positive samples than shell vials (35% vs. 3.7% respectively). IHC staining also aided the pathologist in diagnosing viral infections microscopically. We expect the findings to be instrumental in streamlining not only our institutional SIDS investigation protocol, but also the development of a standardised national SIDS investigation protocol. / AFRIKAANSE OPSOMMING: “Sudden Unexpected Death in Infancy” (SUDI) verwys na enige skielike sterfte van ‘n kind. Indien die kind sterf tydens sy/haar slaap periode en geen oortuigende oorsaak van dood bepaal kan word deur middel van ’n volledige nadoodse ondersoek en ondersoek na die omstandighede tydens die dood, insluitend ’n besoek aan die doodstoneel nie, word so ’n geval as Wiegiedood (SIDS) geklassifiseer. SuidAfrikaanse wetgewing vereis ’n volledige medies-geregtelike nadoodse ondersoek in gevalle waar die oorsaak van dood onbekend is – insluitend gevalle van moontlike Wiegiedood. Daar is min twyfel dat virusinfeksie ‘n oorsaak van, of bydraende faktor tot dood kan wees in gevalle van moontlike SUDI. By die Tygerberg forensiese laboratorium vorm die evaluasie van long weefsel vir die teenwoordigheid van dodelike virusinfeksies deel van die institusionele protokol vir die ondersoek van SUDI gevalle. Long monsters van hierdie SUDI gevalle ondergaan roetine toetse vir die teenwoordigheid van sitomegaalvirus, respiratoriese sinsitialevirus en adenovirus deur middel van selkulture (“shell vial cultures”). In ‘n retrospektiewe steekproef van 366 SUDI gevalle by Tygerberg Hospitaal, Wes-Kaap van 2004 – 2006, is bevind dat in slegs 13.9% van moontlike SUDI gevalle die teenwoordigheid van een of meer van bogenoemde virusse bevestig kon word. Ons hipotese is dat hierdie metode van virus deteksie, tesame met ander faktore soos die tydsinterval tussen dood en nadoodse ondersoek, tyd om monsters na die laboratorium te vervoer ens. moontlik nie optimaal is om ‘n realistiese beeld van dood in babas as gevolg van pulmonale virusinfeksie te gee nie. Aangesien ander toets modaliteite bestaan vir die diagnose van pulmonale virusinfeksies, is hierdie metodes vergelyk in terme van positiewe opbrengs en assosiasie met virale pneumonitis, teen ’n agtergrond van die koste en tyd benodig per toets. ’n Totaal van 82 monsters is oor ‘n 8 maande periode versamel en roetine selkulture is gedoen, gevolg deur “real-time” Polimerase Ketting Reaksie (PKR), asook immunohistochemiese (IHC) kleuring van long snitte met patologiese verslae. Soos vermoed, is gevind dat die real-time PKR metode baie meer akkuraat is om positiewe monsters te identifiseer as roetine selkulture (35% vs 3.7% onderskeidelik). IHC kleuring het ook mikroskopiese diagnose van virale infeksies deur die patoloog vergemaklik. Ons verwag dat hierdie bevindinge grootliks kan bydra in die vaartbelyning van ons institusionele SIDS ondersoek protokol, asook in die ontwikkeling van ’n gestandaardiseerde nasionale SIDS ondersoek protokol.

Overlaying was a common nineteenth century explanation of sudden infant death while bedsharing. This thesis shows that in many cases the term overlaying was a misnomer, and instead it identifies infant overlaying death as a socio-structural historical event that can best be understood within a sociological and social constructionist framework. It expands on the work of Giddens, Elias and Archer to develop a theoretical perspective that incorporates ideas about structuration, sequestration, figuration and reflexivity. It also deploys concepts such as motherhood, infancy, infant care, the family and intimacy to explore and analyse its research materials and develops two further explanatory concepts; reflexive motherhood and the sequestration of infancy. The thesis uses ideas around discourse as socio-structural conditions of action in order to expand current understanding of overlaying death, and it explores and analyses public representations of overlaying during the nineteenth and early twentieth centuries to detail the discourse of overlaying. It goes on to identify cases of overlaying in Somers Town, St Pancras, c1900; and it shows the influence of social conditions in regard to the way such deaths were interpreted. It then examines other cases of sudden infant death in bed through the case notes of pathologist Dr Ludwig Freyberger, and analyses these in terms of the domestic setting and the body. It goes on to detail and analyse a dispute between Coroner John Troutbeck, Dr Freyberger and the GPs of south west London to show the ways in which the overlaying discourse was deployed to support the claims and positions of those involved. Overlaying subsequently became detached from the domestic context in which it was embedded and used to support discourses around infant mortality, maternal ‘ignorance’, medicine, national efficiency and temperance. The thesis provides a historiography of infant overlaying death and concludes that overlaying was constructed as social category of death through the actions of individuals in extensive networks of interdependence in relation to socio-structural conditions.

Wong Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves [110]-126). / Abstracts in English and Chinese. / ABSTRACT --- p.VI / ACKNOWLEDGEMENTS --- p.X / GLOSSARY --- p.XI / Chapter CHAPTER 1 --- INTRODUCTION AND LITERATURE REVIEW --- p.1 / Chapter 1.1 --- Sudden infant death syndrome --- p.1 / Chapter 1.1.1 --- Definition --- p.1 / Chapter 1.1.2 --- Epidemiology of sudden infant death syndrome --- p.1 / Chapter 1.1.3 --- Pathologic findings --- p.5 / Chapter 1.1.4 --- Theories of causation --- p.6 / Chapter 1.1.5 --- Associations of SIDS with temperature and hyperthermia --- p.8 / Chapter 1.1.6 --- Associations of sudden infant death syndrome with infection --- p.11 / Chapter 1.1.7 --- Association of sudden infant death syndrome with sleep state --- p.13 / Chapter 1.2 --- Overview of cytokines --- p.15 / Chapter 1.2.1 --- Definition --- p.15 / Chapter 1.2.2 --- Classification of cytokines --- p.15 / Chapter 1.2.3 --- Biological activities --- p.16 / Chapter 1.2.4 --- Cytokines and temperature --- p.20 / Chapter 1.2.5 --- Cytokines and infection --- p.22 / Chapter 1.2.6 --- Cytokines and smoking --- p.23 / Chapter 1.2.7 --- Cytokines and sleep/arousal --- p.23 / Chapter 1.3 --- Hypothesis and aims of the study --- p.27 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.28 / Chapter 2.1 --- Overview of methods in piglet experiments --- p.28 / Chapter 2.2 --- Pilot study design --- p.30 / Chapter 2.2.1 --- Study Groups --- p.30 / Chapter 2.2.2 --- Temperature controller --- p.33 / Chapter 2.2.3 --- PowerLab system --- p.34 / Chapter 2.2.4 --- Experimental set up --- p.36 / Chapter 2.2.5 --- Provisional ethical approval --- p.36 / Chapter 2.3 --- Problems and results of pilot experiments --- p.37 / Chapter 2.3.1 --- What is baseline body temperature of neonatal rat? --- p.38 / Chapter 2.3.2 --- What type of anaesthesic agent to use? --- p.39 / Chapter 2.3.3 --- What dose of ketamine to use? --- p.40 / Chapter 2.3.4 --- Dilution of ketamine --- p.41 / Chapter 2.3.5 --- Temperature calibration --- p.41 / Chapter 2.3.6 --- What is optimal neonatal rat age to use? --- p.44 / Chapter 2.3.7 --- Which method of blood collection to use? --- p.45 / Chapter 2.3.8 --- What method to raise body temperature? --- p.47 / Chapter 2.3.9 --- Summary results --- p.48 / Chapter 2.4 --- Final study design --- p.49 / Chapter 2.4.1 --- Study animal --- p.49 / Chapter 2.4.2 --- Final Study Groups --- p.50 / Chapter 2.4.3 --- Final ethical approval --- p.56 / Chapter 2.4.4 --- Muramyl dipeptide --- p.56 / Chapter 2.4.5 --- Recalibration of Temperature Controller --- p.57 / Chapter 2.4.6 --- Data collection --- p.58 / Chapter 2.4.7 --- Blood collection and Storage --- p.58 / Chapter 2.4.8 --- Study timetable --- p.59 / Chapter 2.5 --- Cytokines analysis --- p.59 / Chapter 2.5.1. --- Methods of Quantitative Enzyme Immunoassay --- p.59 / Chapter 2.5.2 --- Base theories of Enzyme-linked immunosorbent assay (ELISA) --- p.60 / Chapter 2.5.3 --- Procedure for cytokines assay --- p.61 / Chapter 2.6 --- Histology --- p.65 / Chapter 2.6.1. --- Macroscopic --- p.65 / Chapter 2.6.2. --- Microscopic --- p.65 / Chapter 2.7 --- Data handling and statistical analysis --- p.66 / Chapter CHAPTER 3 --- RESULTS --- p.67 / Chapter 3.1 --- Group (body weight) characteristics --- p.67 / Chapter 3.2 --- Serum concentration of IL- 6，IL-1 β --- p.69 / Chapter 3.3 --- Temperature --- p.78 / Chapter 3.4 --- Mortality rate --- p.80 / Chapter 3.5 --- Cardio-respiratory parameters --- p.85 / Chapter 3.6 --- Macroscopic findings at postmortem --- p.87 / Chapter 3.7 --- Histology --- p.91 / Chapter CHAPTER 4 --- DISCUSSION --- p.96 / Chapter 4.1 --- Study Model --- p.96 / Chapter 4.11 --- Core temperature of newborn rat --- p.95 / Chapter 4.12 --- Temperature calibration --- p.97 / Chapter 4.13 --- Respiratory and pulse rate measurements --- p.93 / Chapter 4.14 --- Measurement of sleep state --- p.99 / Chapter 4.2 --- Animal age and weight --- p.99 / Chapter 4.3 --- Cytokines response to heating --- p.101 / Chapter 4.4 --- Cytokine response to MDP --- p.104 / Chapter 4.5 --- "Hyperthermia, MDP and mortality" --- p.106 / Chapter 4.6 --- Further study --- p.107 / Chapter CHAPTER 5 --- CONCLUSION --- p.109 / Chapter 5.1 --- Small animal model of hyperthermia --- p.109 / Chapter 5.2 --- Hyperthermia and MDP elicit cytokine response --- p.109 / Chapter 5.3 --- Hyperthermia and MDP increase mortality rate --- p.109 / REFERENCES --- p.110 / APPENDICES --- p.A / Appendix 1: Experimental record --- p.A / Appendix 2 : Planned Study Timetable --- p.C / Appendix 3: PowerLab System --- p.E

The purpose of this study was to investigate the time of admission to a Neonatal Intensive Care Unit (NICU) and its association with in-hospital mortality among a cohort of neonates at a regional perinatal center. Two different time points were considered: admissions on the weekend versus the weekday and admissions during the nighttime shift versus the day shift. The secondary purpose of the study was to investigate if registered nurse staffing affected this association between NICU admission day or admission time and in-hospital death. Three separate databases were used which contained information on NICU admissions, hospital deliveries and nurse staffing. These databases were linked resulting in data for each individual mother-infant pair for each separate admission to the NICU. Readmissions to the NICU, NICU admissions which could not be linked with the delivery data, admissions from the Newborn Nursery and transfers from other hospitals were excluded from the study. The final study population consisted of 1,846 admissions from October 1, 2001 through December 31, 2006. Weekend admissions were lower than weekday admissions (29.6% versus 70.4%) and nighttime admissions were lower than day admissions (43.2% versus 56.8%). Infants admitted at nighttime were more likely to be low birth weight, have lower Apgar scores and less likely to be delivered by cesarean section. Weekend admissions did not differ significantly from weekday admissions, except weekend admissions were more likely to be Black (33.6% versus 28.6%, p=.30). After adjusting for infant's acuity and other covariates using multivariate logistic regression, the odds of dying on the weekend was not significantly different than weekday admissions (AOR=1.06, 95% CI=.653-1.721) and were not significantly different for nighttime admissions (AOR=1.14, 95% CI=.722-1.79). Nurse staffing was not a significant covariate. Covariates which were significant risk factors for death prior to discharge were non-Black race of the infant, Apgar score of less than 7 at five minutes, presence of a fetal anomaly, and use of ventilation during the stay. Infant's birth weight was a significant protective factor.